Springfield,IL:CharlesCThomas;1958.)Left vagus nerveRight vagus nerve Right inferior cervical ganglion Right stellate ganglion Recurrent branch of right vagus Vagosympathetic fibers Brachiocephalic artery Baroreceptor fibers Cardiac nerves Aorta Right coronary artery Left inferior cervical ganglion Left subclavian ansa Left subclavian artery Recurrent branch of left vagus Aortic bodies Ductus arteriosus Pulmonary artery Left stellate ganglion Vagosympathetic fibers Vagosympathetic fibers widened areas at the origins of the internal carotid arteries. Impulses that arise in the carotid sinus travel up the carotid sinus nerve (nerve of Hering) to the glossopharyngeal nerve (cranial nerve IX) and, via the latter, to the nucleus of the tractus solitarius (NTS) in the medulla. The NTS is the site of the central projections of the chemoreceptors and baroreceptors. Stimulation of the NTS inhibits sympathetic nerve outflow to the peripheral blood vessels (depressor effect), whereas lesions of the NTS produce vasoconstriction (pressor effect). Impulses that arise in the aortic arch baroreceptors reach the NTS via afferent fibers in the vagus nerves.
Baroreceptor nerve terminals in the walls of the carotid sinus and aortic arch respond to the vascular stretch and deformation induced by changes in arterial blood pressure. The frequency of firing of these nerves is enhanced by an increase in arterial blood pressure and diminished by a reduction in arterial blood pressure. An increase in impulse frequency, as occurs with a rise in arterial pressure, inhibits the cerebral vasoconstrictor regions and results in peripheral vasodilation and lowering of arterial blood pressure. Bradycardia brought about by activation of the cardiac branches of the vagus nerves contributes to this lowering of blood pressure.
The carotid sinus baroreceptors are more sensitive than those in the aortic arch. Changes in carotid sinus pressure evoke greater changes in systemic arterial pressure and peripheral resistance than do equivalent changes in aortic arch pressure.
The receptors in the carotid sinus walls respond more to pulsatile pressure than to constant pressure. This is illustrated in
Fig. 18.27 , which shows that at normal levels 0 0.5 1.0 1.5 2.0 •Fig. 18.27 Relationshipofphasicaorticbloodpressureinthefiring
CHAPTER 18 Regulation of the Heart and Vasculature of mean arterial blood pressure (≈100 mm Hg), a barrage of impulses from a single fiber of the sinus nerve is initiated in early systole by the pressure rise; only a few spikes occur during late systole and early diastole. At lower arterial pressure, these phasic changes are even more evident, but the overall discharge frequency is reduced. The blood pressure threshold for evoking sinus nerve impulses is approxi mately 50 mm Hg; maximal sustained firing is reached at approximately 200 mm Hg. Because the baroreceptors adapt, their response at any mean arterial pressure level is greater to a high pulse pressure than to a low pulse pressure.
The increases in resistance that occur in response to reduced pressure in the carotid sinus vary from one peripheral vascular bed to another. These variations allow blood flow to be redistributed. The resistance changes elicited by altering carotid sinus pressure are greatest in the femoral vessels, less in the renal vessels, and least in the mesenteric and celiac vessels.